1

INVESTOR PRESENTATION

December 2019

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Forward-Looking StatementsThis presentation contains certain “forward-looking” statements that are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. All statements, other than statements of historical or present facts, are forward-looking statements, including statements regarding our future financial condition, future revenues, projected costs, prospects, business strategy, and plans and objectives of management for future operations, including our plans to submit for regulatory filings. In some cases, you can identify forward-looking statements by terminology such as “believe,” “will,” “may,” “might,” “estimate,” “continue,” “anticipate,” “intend,” “target,” “project,” “model,” “should,” “would,” “plan,” “expect,” “predict,” “could,” “seek,” “goal”, “potential,” or the negative of these terms or other similar terms or expressions that concern our expectations, strategy, plans, or intentions. These statements are based on our intentions, beliefs, projections, outlook, analyses, or current expectations using currently available information, are not guarantees of future performance, and involve certain risks and uncertainties. Although we believe that the expectations reflected in these forward-looking statements are reasonable, we cannot assure you that our expectations will prove to be correct. Therefore, actual outcomes and results could materially differ from what is expressed, implied, or forecast in these statements. Any differences could be caused by a number of factors including but not limited to: our expectations regarding the timing, costs, conduct, and outcome of our clinical trials, including statements regarding the timing of the initiation and availability of data from such trials; the timing and likelihood of regulatory filings and approvals for our product candidates; whether regulatory authorities determine that additional trials or data are necessary in order to obtain approval; our ability to obtain funding for our operations, including funding necessary to complete further development and commercialization of our product candidates; our plans to research, develop, and commercialize our product candidates; the commercialization of our product candidates, if approved; the rate and degree of market acceptance of our product candidates; our expectations regarding the potential market size and the size of the patient populations for our product candidates, if approved for commercial use, and the potential market opportunities for commercializing our product candidates; the success of competing therapies that are or may become available; our expectations regarding our ability to obtain and maintain intellectual property protection for our product candidates; the ability to license additional intellectual property relating to our product candidates and the comply with our existing license agreements; our ability to maintain and establish relationships with third parties, such as contract research organizations, suppliers, and distributors; our ability to maintain and establish collaborators with development, regulatory, and commercialization expertise; our ability to attract and retain key scientific or management personnel; our ability to grow our organization and increase the size of our facilities to meet our anticipated growth; the accuracy of our estimates regarding expenses, future revenue, capital requirements, and needs for additional financing; our expectations related to the use of our available cash; our ability to develop, acquire, and advance product candidates into, and successfully complete, clinical trials; the initiation, timing, progress, and results of future preclinical studies and developments and projections relating to our competitors and our industry.

Additional factors that could cause actual results to differ materially from our expectations can be found in our Securities and Exchange Commission filings. Moreover, we operate in a very competitive and rapidly changing environment. New risk factors emerge from time to time, and it is not possible for our management to predict all risk factors, nor can we assess the effects of all factors on our business or the extent to which any factor, or combination of factors, may cause actual results to differ materially from those contained in, or implied by, any forward-looking statements. All forward-looking statements included in this presentation are expressly qualified in their entirety by these cautionary statements. The forward-looking statements speak only as of the date made and, other than as required by law, we undertake no obligation to publicly update or revise any forward-looking statements, whether as a result of new information, future events, or otherwise.

Bardoxolone methyl and omaveloxolone are investigational drugs, and their safety and efficacy have not been established by any agency.

3

Reata at a Glance

Global Opportunity

• Reata possesses WW commercial rights to all pipeline assets*

• Few or no effective therapies currently approved for lead indications

Bardoxolone in Rare Forms of CKD

• Positive pivotal data in Alport

syndrome

• Pipeline in rare forms of CKD

• Pivotal ADPKD study ongoing

• Positive proof-of-concept data in

FSGS, IgAN, and T1D-CKD

Omaveloxolone in Neurology

• Positive pivotal data in FA

• Proof-of-concept in other

neurological diseases

• Plan to study Omav in additional

indications

*ex-Asia for Bardoxolone

4

DISCOVERY PRECLINICAL PHASE 1 PHASE 2 PIVOTAL NDA

CKD Caused by Alport Syndrome | Bard

Friedreich’s Ataxia | Omav

IgA Nephropathy | Bard

Type 1 Diabetic CKD | Bard

Focal Segmental Glomerulosclerosis | Bard

Neurological Indications | RTA 901

Autoimmune Indications | RTA 1701

Connective Tissue Disease-Associated Pulmonary Arterial Hypertension | Bard

Deep Pipeline With Two Pre-Registration Programs and

Two Pivotal Studies Ongoing

Autosomal Dominant Polycystic Kidney Disease | Bard

5

BardoxoloneChronic Kidney Disease

6

Bard Development for Rare Forms of CKD

CARDINAL Phase 3 study in Alport syndrome met its primary and key secondary endpoints

Significant opportunity in rare forms of CKD‒ We estimate aggregate prevalence exceeds

700,000 patients in the US

‒ Few or no effective therapies currently approved

FALCON Phase 3 study in ADPKD‒ FALCON design and endpoints similar to

CARDINAL Phase 3 study

‒ Initiated in May 2019

Positive data from PHOENIX in IgAN, FSGS and T1D CKD; planning to pursue commercially

US Rare CKD Patients

ADPKD 5

T1D CKD 4

FSGS2

IgAN 3

Alport

Syndrome1

~400,000

~160,000

~120,000

~40,000

~30,000-

60,000

1Alport Syndrome Foundation; Estimated based on Persson Clin Nephrol (2005); USRDS Report; Hasstedt Am J Hum Genet. (1983); Temme, Kidney Int. (2012); 2Wetmore (2016), Sim (2016); 3Berthoux (2011), Wetmore (2016), Sim (2016); 4American Diabetes Association, Garofolo (2018), Ohta (2010); 5PKD Foundation

7

Alport Syndrome is a Severe, Inherited Form of CKD

Estimated Prevalence5

Alport syndrome is the second most common

inherited cause of kidney failure1,2

Collagen mutations drive mitochondrial dysfunction,

inflammation, and fibrosis3,4

In most severe forms of disease, median age for

kidney failure is 25 years1

Progressive loss of kidney function leads to need for

dialysis or kidney transplant

1Jais et al., JASN (2000); 2Kashtan et al., Kidney Int (2018); 3Suh et al., Nat Rev Nephrol (2013); 4Gomez et al., JCI (2015); 5Alport Syndrome Foundation; Estimated based on Persson Clin Nephrol (2005); USRDS Report; Hasstedt Am J Hum Genet. (1983); Temme, Kidney Int. (2012)

30,000-60,000

in US

32,000-64,000

in the EU5

Very severe form of CKD with no approved therapies

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CARDINAL Phase 3: Pivotal Study Design

International, double-blind, placebo-controlled, randomized, registrational trial

Largest interventional study in patients with AS

Enrolled a wide and representative range of patients with AS‒ eGFR: 30 to 90 ml/min

‒ Age: 12 to 70 years

Endpoints: eGFR Improvement on and off treatment‒ Primary: change from baseline in eGFR versus placebo at Week 48

‒ Key Secondary: change from baseline in eGFR versus placebo at Week 52 after withdrawal of drug for 4 weeks

After 52 weeks, patients restart study drug with original treatment assignments and continue for the second year

FDA guided Reata that retained eGFR benefit versus placebo at one year of treatment may support accelerated approval and after two years may support full approval

R

Bard

Placebo

Bard

Placebo

Year 1 On-Treatment Year 2 On-TreatmentW/D W/D

Off

Study

Drug

Off

Study

Drug

1:1

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CARDINAL Met the Primary Endpoint

Bard treatment significantly improved on-treatment eGFR at Week 48 by 9.50 ml/min relative to placebo (p<0.0001)

Placebo patients had significant kidney function loss versus baseline (p=0.0002)*

Bard significantly improved eGFR (p=0.0004)* versus baseline

-4.78

4.72

-8

-6

-4

-2

0

2

4

6

8

Me

an

±S

E e

GF

R C

ha

ng

e (

ml/

min

)

Placebo (n=80) Bardoxolone Methyl (n=77)

p<0.0001

Primary Endpoint:

eGFR Change at Week 48

*p-value estimated comparing the mean changes to zero.

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CARDINAL Met Key Secondary Endpoint

Bard treatment significantly improved off-treatment eGFR at Week 52 by 5.14 ml/min relative to placebo (p=0.0012)

Placebo patients had significant kidney function loss relative to baseline (p<0.0001)*

Bard patients had a slight, non-significant decline relative to baseline (p=0.45)*

Similar efficacy observed across multiple subgroups, including males versus females, pediatric population, and baseline ACR

-6.11

-0.96

-8

-7

-6

-5

-4

-3

-2

-1

0

Me

an

±S

E e

GF

R C

ha

ng

e (

ml/

min

)

Placebo (n=80) Bardoxolone Methyl (n=77)

p=0.0012

Key Secondary Endpoint:

eGFR Change at Week 52

*p-value estimated comparing the mean changes to zero.

ANCOVA analyses include off-treatment eGFR values

from patients that discontinued treatment early

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Bard Treatment Produced Benefit Across All Quartiles

of Response

Week 48 eGFR Change

Mean ± SD

Week 52 eGFR Change

Mean ± SD

∆eGFR

QuartilePlacebo Bard Placebo Bard

1 4.2 ± 2.4 20.9 ± 11.5 5.0 ± 4.2 12.9 ± 8.1

2 -1.3 ± 1.4 9.2 ± 2.4 -2.5 ± 1.4 2.5 ± 1.6

3 -5.7 ± 1.5 1.7 ± 2.2 -7.4 ± 2.3 -3.2 ± 1.7

4 -16.1 ± 6.4 -10.5 ± 6.4 -17.3 ± 5.0 -12.7 ± 5.6

eGFR change measured as mL/min

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Summary of Safety

Fewer SAEs reported in Bard patients

No fluid overload or major adverse cardiac events in patients treated with Bard

Blood pressure decreased relative to baseline in the Bard group but was not significantly different between groups

Overall low rate of cardiac and vascular AEs that was reduced in the Bard arm

Most common AEs included muscle spasms and increased ALT or AST

Albuminuria increased with Bard at Week 48 but was unchanged when adjusted for eGFR and unchanged from baseline at Week 52

No individual AE contributed to more than two discontinuations in either group

Placebo

(n=80)

Bard

(n=77)

Number of Patients with AE 73 (91%) 75 (97%)

Number of Patients with SAE 10 (13%) 4 (5%)

Number of Patients with AE

Leading to Permanent

Treatment Discontinuation

4 (5%) 9 (12%)

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FALCON Phase 3 Trial of Bard for ADPKD

Pivotal Phase 3 will enroll approximately 300 patients‒ Randomized, double-blind, placebo-controlled international study

‒ Two-year total treatment duration

‒ Planning to enroll patients across approximately 60 sites in the US, Europe, and Australia

Broad eligibility criteria‒ eGFR 30-90 ml/min

‒ Age 18-70 years old

Retained eGFR benefit endpoints support approval‒ Potential accelerated approval on retained eGFR after one year of treatment and drug withdrawal

‒ Potential full approval on retained eGFR after two years of treatment and drug withdrawal

Trial initiated in May 2019

Week12 Week 48 Week 52

Off

Study Drug

Week 100

Baseline UACR ≤ 300 mg/g

Baseline UACR > 300 mg/g

Week 104

Off

Study Drug

Day 1

W/D

Placebo Placebo

Bard: 5 mg

Bard: 5 mg 10 mg

10 mg 20 mg 30 mg

20 mg

Bard: 30 mg

Bard: 20 mg

R

Screen Dose-Titration Period Maintenance W/D Maintenance

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All PHOENIX Cohorts: Bard Significantly Improved

eGFR

Bard significantly increased eGFR by 7.8 ml/min at Week 12

High consistency of response – eGFR increased in 88% of patients at Week 12

Improvements across multiple forms of CKD suggest that Bard is addressing a common, final pathway of progression in CKD

1Defined as proportion of patients reaching Week 12 with eGFR values above baseline at Week 12

0

2

4

6

8

10

0 4 8 12

Mean

±S

E e

GF

R C

han

ge (

mL

/min

)

Study Week

All PHOENIX Cohorts (n=103)

+7.8 ml/min

p<0.00001

Cohort

Week 12

∆eGFR

(ml/min)

ADPKD 9.3 (p<0.0001)

IgAN 8.0 (p<0.0001)

T1D CKD 5.5 (p=0.02)

FSGS 7.8 (p=0.003)

All 7.8 (p<0.00001)

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CKD Program: Summary and Next Steps

The Phase 3 portion of CARDINAL met its primary endpoint (p<0.0001)

The Phase 3 portion of CARDINAL met its precedented, registrational key secondary endpoint (p=0.0012)

Planning to meet with FDA and other regulatory agencies to discuss marketing application submission plans

Beginning to plan for ex-US launch as a result of recent reacquisition of global rights

Pivotal study in ADPKD (FALCON) launched in May 2019

Pivotal study in diabetic kidney disease (AYAME) ongoing in Japan and being conducted by Kyowa Kirin Co, Reata’s licensee

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OmaveloxoloneFriedreich’s Ataxia

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Friedreich’s Ataxia Overview

1 Parkinson MH, et al., J Neurochem. 2013; 52Santos R, et al., Antioxid Redox Signal. 2010; 3Klockgether T, et al., Brain. 1998

Estimated Prevalence

~5,000

in US

~22,000

Globally

Friedreich’s ataxia (FA) is a rare, debilitating, life-

shortening, neuromuscular disorder

Most patients diagnosed as children and survive

into their mid-30s1-3

Numerous failed trials and no approved therapies

Patients typically become wheelchair-dependent

10 to 15 years after diagnosis and eventually lose

independence

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MOXIe Design and Results

International, double-blind, placebo-controlled, randomized, registrational trial

Largest global interventional study in patients with FA

Enrolled a wide and representative range of patients with FA‒ Baseline mFARS: 20 to 80

‒ Age: 16 to 40 years

Patients randomized 1:1 to receive 150 mg Omav or placebo for 48 weeks

Primary endpoint: change from baseline in mFARS at Week 48

IMPROVEDNeurological Function

WORSENEDNeurological FunctionPlacebo

Omav

Difference=2.40

(p=0.014)

Primary Endpoint: Change in mFARS at Week 48

-1.55pt

+0.85pt

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mFARS Improved Over Time

Worsened

Improved

-1.55 pts

+0.85 pts

-2.0

-1.0

0.0

1.0

0 12 24 36 48

Ch

an

ge

fro

m B

as

eli

ne

in

mFA

RS

Study Week

Placebo (n=42) Omav (n=40)

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Omav Improved Several Secondary Endpoints

Improvements observed in Patient Global Impression of Change (PGIC)

‒ Primary analysis population (n=82; p=0.125)

‒ All randomized population (n=103; p=0.028)

‒ Patient-reported PGIC correlated with physician-assessed changes in mFARS (p<0.001)

Activities of Daily Living score achieved nominal significance versus placebo (n=82; p=0.042)

65% reduction in frequency of falls

Activities of Daily Living

SectionImproved with

Omav1

Speech ✓

Swallowing ✓

Cutting Food and Handling Utensils ✓

Dressing ✓

Personal Hygiene ✓

Falling ✓

Walking ✓

Quality of Sitting Position ✓

Bladder Function ✓

Total✓

(p=0.042)

1 All sections demonstrated numerical improvements relative to placebo

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MOXIe Summary of Safety

AEs generally mild to moderate in intensity‒ 4 (8%) Omav patients and 2 (4%) placebo

patients discontinued study due to AEs

‒ ALT and AST increases are a pharmacological effect of Omav1

• Not associated with liver injury

• Coincide with decreases in total bilirubin

• May reflect improvements in mitochondrial metabolism

Low rate of serious AEs (SAEs)‒ SAEs reported in 3 (6%) Omav patients and 3

(6%) placebo patients while receiving study drug

‒ Two additional Omav patients reported SAEs approximately 2 weeks after receiving final dose

Ninety-eight percent of patients chose to enroll in the long-term extension study

1Miller et al., ASN 2010

Summary of Adverse Events*

*AEs reported in >20% of patients

Preferred TermPlacebo

(n=52)

Omav

(n=51)

Contusion 19 (37%) 17 (33%)

Headache 13 (25%) 19 (37%)

Upper respiratory

tract infection15 (29%) 14 (28%)

Excoriation 12 (23%) 13 (26%)

Nausea 7 (14%) 17 (33%)

ALT increased 1 (2%) 19 (37%)

Fatigue 7 (14%) 11 (22%)

Abdominal pain 3 (6%) 11 (22%)

AST increased 1 (2%) 11 (22%)

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Omav Pharmacology May Be Applicable to Broad Set of

Neurodegenerative Diseases

MOXIe results provide proof of concept for use of Omav in other neurodegenerative diseases

Mitochondrial dysfunction and neuroinflammation are common features of FA and other neurodegenerative diseases

Omav and analogs have demonstrated broad activity in neurodegenerative models

‒ Huntington’s Disease

‒ ALS

‒ Parkinson’s Disease

‒ Alzheimer’s Disease

‒ Epilepsy

Yang et al., PLoS One (2009); Neymotin et al., Free Rad Bio (2011); Dinkova-Kostova et al., (2015)Stack et al., Free Rad Biol Med 49 (2010); Dumont et al., J Neurochem (2009); Kim et al., Cells (2019); Shekh-Ahmad, et al., Brain (2018); Wei et al., Sci Rep (2017)

23

BardoxoloneCTD-PAH

24

Bard in Development for Connective Tissue Disease-

Associated Pulmonary Arterial Hypertension

CTD-PAH is an autoimmune form of PAH‒ Affects 10% to 15% of scleroderma and lupus

patients and is their leading cause of death

‒ Estimated prevalence: 12,000 in US; 50,000 worldwide; 30% of all PAH

Despite available therapies, large unmet need‒ Vasodilators are the only current treatment option

and have lower benefit in CTD-PAH versus idiopathic PAH

‒ Vasodilators produce side effects that include syncope, headache, flushing, and jaw pain

‒ Poor risk-benefit for vasodilators in CTD-PAH given minimal treatment effect and adverse events resulting from systemic vasodilation

25

CATALYST is a Global Pivotal Trial of Bard for

Treatment of CTD-PAH

Phase 3 enrollment is complete at 202 patients‒ Randomized, double-blind, placebo-controlled international study

‒ 24-week treatment duration

Broad eligibility criteria‒ 6MWD ≥ 150 meters

‒ Age 18-75 years old

‒ WHO Functional Class II and III on up to two background therapies

6MWD endpoint supports approval‒ Potential full approval on 6MWD after 24 weeks of treatment

‒ Conservatively powered

Data expected mid-2020

Placebo

Bard: 10 mg

R

Day 1 Week24

Bard: 5 mg

Screen Dose-Titration Maintenance

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LARIAT Phase 2 Results: Large Increase in 6MWD

Enrolled idiopathic PAH and CTD-PAH patients and treated for 16 weeks‒ PAH patients required to be on 1 to 2 background therapies

‒ Assessed safety and change in 6MWD

Primary efficacy analysis of initial cohorts presented at CHEST 2015 showed a placebo-corrected 6MWD of 21 m (p=0.037) at doses of 2.5, 5, and 10 mg

Subset of patients with CTD-PAH demonstrated largest responses‒ Clinically meaningful improvement of 28.4 m observed across all patients

‒ Patients without anemia demonstrated a larger placebo-corrected difference of 48.5 m

‒ Patients with anemia at baseline demonstrated larger variability and are excluded in CATALYST

Dataset Treatment N

Week 16 Δ6MWD (m)

Change from

Baseline

Placebo-

corrected

All

Placebo 79.8

p=0.44-

Bard 1538.2

p<0.001

28.4

p=0.07

Without

Anemia

Placebo 5-5.8

p=0.68-

Bard 1442.7

p<0.001

48.5

p=0.005

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Recent Highlights and Key Upcoming Milestones

Bard in Alport syndrome

Positive, one-year pivotal data reported

Omav in Neurology

Positive pivotal data reported in Friedreich’s ataxia

Next neurological indications to be determined

Bard in ADPKD

Pivotal Phase 3 trial in ADPKD initiated in May 2019

Bard in CTD-PAH

Phase 3 CATALYST pivotal data available in mid-2020

Partner Program: Bard in diabetic CKD

Phase 3 AYAME trial fully enrolled, data available in 1H22

Sponsored by Kyowa Kirin Co, Reata’s licensee in Asia

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APPENDIX

29

BARDOXOLONE METHYL OMAVELOXOLONE

Reata Patent Portfolio

Morphic form patent US 8,088,824 claims commercial (amorphous) forms of Bard

Claims granted in US, EU, Japan, Canada, China, Mexico, Eurasia, and 10 other territories with applications pending in 7 other countries

Anticipated protection to 2034 in US and 2033 in rest of world with term extensions

Composition of matter patent (US 8,993,640) claims Omav and several solid forms

Granted in US, Europe, Japan, China, Eurasia, 14 other territories and pending in 13 other countries

Anticipated protection to 2035 in US and 2036 in EU and Japan with term extensions

Genus patent (US 8,124,799) claims granted in 17 foreign territories & pending in 1 more

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Tolvaptan Also Only Slows the Rate of eGFR Decline

-3.61 -2.34

-4

-3

-2

-1

0

Mean

±S

E e

GF

R C

han

ge (

ml/

min

)

Placebo Tolvaptan

1.27 mL/min

Tolvaptan in ADPKD

Retained eGFR Benefit1Tolvaptan recently approved for ADPKD using eGFR change after withdrawal of drug, the retained eGFR benefit

Same registrational endpoint as CARDINAL Phase 3 study

In its registrational REPRISE study, tolvaptan slowed, but did not stop eGFR decline

‒ eGFR in both tolvaptan and placebo groups declined

‒ The tolvaptan group eGFR declined by 2.34 mL/min

‒ The placebo group eGFR declined by 3.61 mL/min

Tolvaptan was approved based on the 1.27 mL/min improvement compared to placebo

1Torres, NEJM (2017)

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Alport Syndrome Patients Rapidly Progress to ESKD

-1.8 -2.0-2.3

-6.1

-7

-6

-5

-4

-3

-2

-1

0

Av

era

ge K

idn

ey F

un

cti

on

De

clin

e(m

l/m

in/1

.73m

2/y

ear)

Diabetic

CKD1

Hypertensive

CKD2 ADPKD3

Alport4

Syndrome

Average Annual Kidney Function Decline

on Standard of Care

1Perkovic et al. 2018 CANVAS; 2Wright et al. 2002 AASK; 3Torres et al. 2017 REPRISE; 4CARDINAL Phase 3 placebo arm5Assuming baseline eGFR=60 mL/min and ESKD occurs at 15 mL/min

Estimated Years

to ESKD5 25 23 19 7

32

CARDINAL Phase 2 Results: Urinary Protein Not

Significantly Changed at Weeks 48 or 52

Injury due to hyperfiltration would cause UACR to increase over time

UACR not significantly different from baseline at Weeks 48 or 52‒ Initial increase in UACR explained by increase in GFR

‒ After initial eGFR-based increase, UACR trends down through Week 48

‒ Mean changes clinically insignificant

Patients with baseline UACR > 300 mg/g (n=9) had 10% reduction at Week 48 and 28% reduction at Week 52

1Uses log-transformation methodology adopted by NKF/FDA/EMA Scientific Working Group to compute changes in albuminuria2KDIGO (Kidney Disease Improving Global Outcomes) 2013 classification of albuminuria

A1: Normal (<30)

UACR Categories2

A2: Microalbuminuria (30-300)

A3: Macroalbuminuria (>300)

Nephrotic (>3,500)UACR Over Time1

0

200

400

600

800

1000

1200

1400

1600

0 8 16 24 32 40 48 56

Geo

metr

ic M

ean

U

AC

R (

mg

/g)

Study Week

All Patients (n=25)

Baseline UACR>300 mg/g (n=9)

W/D

33

Retained eGFR Benefit is an Accepted Approvable

Endpoint in Rare CKD Trials

Withdrawal of drug after long-term treatment provides evidence whether an intervention protected or harmed the kidney during treatment

For pivotal trials, FDA has accepted or required retained benefit analyses in ADPKD, Alport syndrome, IgAN, and FSGS

The duration of withdrawal does vary by drug and is based on its PK/PD profile‒ Time required for the drug to reach sub-therapeutic concentrations

‒ Time needed for reversal of PD markers

‒ Dosing duration required for maximal effect

Trial Company Drug Disease Phase

REPRISE Otsuka Tolvaptan ADPKD Approved

FALCON Reata Bardoxolone ADPKD Phase 3

CARDINAL Reata Bardoxolone Alport syndrome Phase 3

PROTECT Retrophin Sparsentan IgA Nephropathy Phase 3

ARTEMIS-IGAN Omeros OMS721 IgA Nephropathy Phase 3

DUPLEX Retrophin Sparsentan FSGS Phase 3

34

Four Week Off-Treatment Duration is Sufficient to

Assess Retained Benefit with Bard

Bard’s maximal effect on eGFR after initiation of dosing occurs within 2-4 weeks after the last increase in dose

Bard is eliminated within 2 weeks after cessation of dosing‒ 4-week withdrawal represents approximately 17 half-lives of drug

‒ Sub-therapeutic concentrations are achieved with no active metabolites

‒ Pharmacodynamic markers of Nrf2 activation, which are monitored in all patients, are not significantly different from baseline after 4-week withdrawal

Post-treatment eGFR values stabilize by Week 4 in T2D CKD patients

BEACON: eGFR Changes are Maximal 4 Weeks

After the Last Increase in Dose

Mean Baseline and Change in

eGFR (mL/min)Placebo Bard

Baseline 22.5 22.4

Change 4 weeks post-last dose 2.1

Change 8 weeks post-last dose 2.4

BEACON: Post-treatment eGFR Relatively Stable

through 8 Weeks Following Cessation of Bard Treatment

15.0

20.0

25.0

30.0

35.0

0 4 8 12 16 20 24 28 32 36 40 44 48

Mean

eG

FR

±S

E (

ml/

min

/1.7

3 m

2)

Treatment Week

PBO

BARD

35

List of Abbreviations

6MWD Six-minute walk distance

ADPKD Autosomal dominant polycystic kidney disease

ACEi Angiotensin-converting enzyme inhibitor

ALS Amyotrophic lateral sclerosis

ARB Angiotensin receptor blocker

AS Alport syndrome

ATP Adenosine triphosphate

Bard Bardoxolone methyl

CKD Chronic kidney disease

CTD-PAH Connective tissue disease-associated pulmonary arterial hypertension

eGFR Estimated glomerular filtration rate

EOP2 End-of-Phase 2 meeting

ESKD End-stage kidney disease

FA Friedreich’s Ataxia

FDA US Food and Drug Administration

FSGS Focal segmental glomerulosclerosis

GBM Glomerular basement membrane

GFR Glomerular filtration rate

IgAN IgA nephropathy

KHK Kyowa Hakko Kirin Co. Ltd.

mFARS Modified Friedreich’s ataxia rating scale

mL/min mL/min/1.73 m2

NDA New drug application

Nrf2 Nuclear factor (erythroid-derived 2)-related factor 2

Omav Omaveloxolone

PAH Pulmonary arterial hypertension

PBO Placebo

PK/PD Pharmacokinetics/pharmacodynamics

SOC Standard of Care

T1D CKD Type 1 diabetic chronic kidney disease

T2D CKD Type 2 diabetic chronic kidney disease

UACR Urinary albumin to creatinine ratio

W/D Withdrawal